Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy [miR146aKO_ESLAM_SCBS]

ABSTRACT: Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy [miR146aKO_ESLAM_SCBS]

PROVIDER: PRJNA626673 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11576300_1.fastq.gz	Fastqsanger.gz
	SRR11576300_2.fastq.gz	Fastqsanger.gz
	SRR11576301_1.fastq.gz	Fastqsanger.gz
	SRR11576301_2.fastq.gz	Fastqsanger.gz
	SRR11576302_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 138

Similar Datasets

Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy [miR146aKO_ESLAM_SCBS]

Project description:Aging is associated with significant changes in the hematopoietic system, including increased inflammation, impaired hematopoietic stem cell (HSC) function, and increased incidence of myeloid malignancy. Inflammation of aging (“inflammaging”) has been proposed as a driver of age-related changes in HSC function and myeloid malignancy, but mechanisms linking these phenomena remain poorly defined. Here, we identify loss of miR-146a as driving aging-associated inflammation in AML patients. miR-146a expression declined in old wild-type mice, and loss of miR-146a promoted premature HSC aging and inflammation in young miR-146a-null mice, preceding development of aging-associated myeloid malignancy. Using single-cell assays of HSC quiescence, stemness, differentiation potential, and epigenetic state to probe HSC function and population structure, we found that loss of miR-146a depleted a subpopulation of primitive, quiescent HSCs. DNA methylation and transcriptome profiling implicated NF-κB, IL6, and TNF as potential drivers of HSC dysfunction, activating an inflammatory signaling relay promoting IL6 and TNF secretion from mature miR-146a-/- myeloid and lymphoid cells. Reducing inflammation by targeting Il6 or Tnf was sufficient to restore single-cell measures of miR-146a-/- HSC function and subpopulation structure, and reduced the incidence of hematological malignancy in miR 146a-/- mice. miR-146a-/- HSCs exhibited enhanced sensitivity to IL6 stimulation, indicating that loss of miR-146a affects HSC function via both cell-extrinsic inflammatory signals and increased cell-intrinsic sensitivity to inflammation. Thus, loss of miR 146a regulates cell-extrinsic and -intrinsic mechanisms linking HSC inflammaging to the development of myeloid malignancy.

2020-05-14 | GSE148988 | GEO

Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy [miR146aKO_LSK_WGBS]

2020-05-14 | GSE148989 | GEO

Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy

Project description:Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy

| PRJNA627370 | ENA

Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy [miR146aKO_LSK_WGBS]

Project description:Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy [miR146aKO_LSK_WGBS]

| PRJNA626672 | ENA

Altered microRNA expression links IL6 and TNF-induced inflammaging with myeloid malignancy

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-05-14 | GSE149097 | GEO

MDMs Solvent, AA, IL6, AA+IL6

Project description:MDMs Solvent, AA, IL6, AA+IL6

| PRJEB36942 | ENA

Effect of anti-TNF/IL-6 NANOBODY® VHH, Humira, Sylvant, TNF, IL6 and TNF+IL6 in RA-FLS/T cell cocultures

Project description:Additive effects of TNF and IL-6 were evaluated in cell-based model for rheumatoid arthritis (RA) and then compared to treatment with anti-TNF/IL-6 NANOBODY® VHH, Humira and Sylvant by RNA-seq

2022-12-31 | GSE200291 | GEO

Organ-specific inflammaging in mice

Project description:Aging is accompanied by chronic, low-grade systemic inflammation, termed inflammaging, a main driver of age-associated diseases. Such sterile inflammation is typically characterized by elevated levels of pro-inflammatory mediators, such as cytokines and reactive oxygen species causing organ damage. Lipid mediators play important roles in the fine-tuning of both the promotion and the resolution of inflammation. Yet, it remains unclear how lipid mediators fit within the concept of inflammaging and how their biosynthesis and function is affected by aging. Here, we provide comprehensive signature profiles of inflammatory markers in organs afflicted with inflammation of young and old C57BL/6 mice. We reveal an organ-specific footprint of inflammation-related cytokines, chemokines and lipid mediators, which are distinctively affected by aging. While some organs are characterized by a pronounced pro-inflammatory microenvironment and impaired resolution during aging, others display elevated levels of pro-resolving mediators or an overall decrease in inflammatory signaling. Our results demonstrate that it proves difficult to establish a unifying concept for alterations of immunomodulatory mediators as consequence of aging and that organ specificity needs to be considered. Moreover, our data imply that inclusion of lipid mediators into the concept of inflammaging provides a comprehensive tool to characterize the inflammatory microenvironment during aging on a broader and yet, more detailed scope.

2021-03-22 | PXD024356 | Pride

Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice [ATAC_invivo]

Project description:Low-grade chronic inflammation is considered a hallmark of ageing and associated with impaired tissue function and development of disease. However, how cell-intrinsic and -extrinsic factors interact to establish this phenotype, termed inflammaging, remains poorly understood. We addressed this question in the mouse intestinal epithelium, using organoid cultures to dissect stem cell-intrinsic and -extrinsic sources of increased inflammatory signaling upon ageing. At the single-cell level, we found that inflammaging establishes differently in cells along the crypt-villus axis, including intestinal stem cells (ISCs). Importantly, the inflammaging phenotype was stably propagated by aged ISCs in organoid cultures and associated with increased chromatin accessibility of inflammation-associated loci in vivo and ex vivo, indicating a cell-intrinsic memory of inflammation. Mechanistically, we show that expression of inflammaging genes is dependent on STAT1 signaling. Together, our data reveal that inflammaging in the intestine is promoted by a cell-intrinsic mechanism, stably propagated by ISCs and associated with a disbalance in immune homeostasis.

2023-10-26 | GSE233898 | GEO